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Biomedical subjects

D G Pace

Publications and source records attributed to D G Pace.

9 recordsLinked to original sources
PubMed1988

Evaluation of methods of administering tyramine to raise systolic blood pressure.

To compare the relative merits of two different administration regimens, tyramine was administered intravenously in ascending doses to 12 healthy subjects to raise systolic blood pressure slightly more than 30 mm Hg. Six subjects received tyramine by bolus injection and six other subjects received tyramine by infusion. The bolus dose of tyramine needed was 4.34 +/- 1.51 mg (X +/- SD) and the infusion rate needed was 1.11 +/- 0.33 mg/min. Four blood pressure response patterns to continuous tyramine infusion were observed. Because different units were measured for the quantity of tyramine administered, the between-subject variance estimate to within-subject variance estimate ratios were calculated. The two techniques had equivalent consistency. With the bolus method, in contrast to the infusion procedure, the dose-response relationship was obvious in most subjects. Therefore the bolus method was judged to be more useful than the infusion method.

Adult↗
PubMed1987

Inhibitory control of proximal colonic motility by the sympathetic nervous system.

The purpose of this study is to determine whether or not the sympathetic nervous system provides a tonic inhibitory input to the colon in chloralose-anesthetized cats. Proximal and midcolonic motility were monitored using extraluminal force transducers. An intravenous bolus injection of 5 mg of phentolamine in 14 animals elicited a pronounced increase in proximal colon contractility. The minute motility index changed from 0 +/- 0 to 26 +/- 4 after phentolamine administration. Midcolonic motility also increased in response to phentolamine. Specific blockade of alpha 2-receptors, but not alpha 1-receptors, caused the same response seen with phentolamine. alpha-Adrenergic blockade increased colon contractility after spinal cord transection but not after ganglionic blockade. Blockade of alpha-adrenergic receptors was also performed before vagal and pelvic nerve stimulation and in both cases increased colonic motility. Vagal stimulation alone had no effect on colonic contractility, while pelvic nerve stimulation increased motility at the midcolon. alpha-Receptor blockade did not alter the ineffectiveness of vagal stimulation but did unmask excitatory effects of pelvic nerve stimulation on the proximal colon. All excitatory colonic responses were prevented by blocking muscarinic cholinergic receptors. These data indicate that tonic sympathetic nervous system activity exerts an inhibitory effect on colonic motility. The inhibitory effect is mediated through alpha 2-adrenergic receptors. Based on these findings, we suggest that alterations in sympathetic nervous system activity may be extremely important for the regulation of circular muscle contractions in the colon.

Acetylcholine↗
PubMed1985

Effect of brief bursts of carotid sinus stimuli on heart rate and atrioventricular conduction.

The effect of a single brief stimulus burst applied simultaneously to both carotid sinus nerves on atrioventricular conduction (PR) was examined in paced and unpaced preparations of anesthetized open-chest dogs. The relative timing of the stimulus burst was varied to encompass the complete cardiac cycle. Carotid sinus/vagal effect curves were constructed to identify the time course of the response. In paced preparations the maximum increase in PR was 20.3 +/- 2.7 msec and this occurred 458.0 +/- 22.8 msec after the stimulus. There was a latency of 246.0 +/- 12.4 msec after the electrical stimulus before the PR began to increase. In unpaced heart preparations the effect of single carotid sinus nerve stimuli on heart period (PP) and PR was also determined. PP was maximally lengthened by 251.4 +/- 49.4 msec at 644.2 +/- 50.9 msec after the stimulus. There was a latency of 251.4 +/- 10.5 msec before the first noticeable change in PP occurred. The PR response was biphasic. The maximum lengthening of the PR interval was 16.2 +/- 4.2 msec. This response occurred at 361 +/- 22.0 msec after the electrical stimulus. The PR decreased to a minimum value of 13.6 +/- 2.2 msec below control values at 767.1 +/- 44.0 msec after the stimulus. The overall effect of carotid sinus activity on atrioventricular conduction depends not only on the direct nodal effect of acetylcholine but also on the indirect heart rate changes. We conclude that brief bursts of carotid sinus nerve stimulation produce cardiac electrophysiological effects qualitatively similar to the effects of direct vagal stimulation, differing only in having a lower amplitude, a longer latency and a somewhat wider time dispersion.

Animals↗
PubMed1979

Digoxin-induced decrease in intraocular pressure in the cat.

A constant intravenous infusion of digoxin (2 micrograms/kg/min) to alpha-chloralose-anesthetized cats produced a progressive decrease in intraocular pressure with increasing doses of digoxin between 60 micrograms/kg and drug-induced ventricular arrhythmia which occurred at a mean dose of 172 micrograms/kg. Digoxin elicited a 40% decrease in intraocular pressure just prior to ventricular arrhythmia compared to a decrease of only 10% with a control infusion of diluent in the same animal (P less than 0.05). There was no significant difference (P less than 0.1) between changes in blood pressure and heart rate observed in the experimental versus the control infusions. The decrease in intraocular pressure may result from inhibition of the Na-K-ATPase in the ciliary body.

Animals↗
PubMed1978

Interactions between digoxin and brief vagal bursts influencing atrioventricular conduction.

The interaction between intravenous injections of digoxin (20 microgram/kg every 15 minutes) and brief electrical bursts of vagal stimulation was determined in chloralose-anesthetized dogs. Vagal effect curves were generated to characterize the effect of brief vagal stimulus bursts on atrioventricular conduction. These curves were fit with an analytic expression from which the following parameters were derived as the experimental observations: 1) the maximal change in atrioventricular conduction (deltaPRmax), 2) the time after the stimulus at which atrioventricular conduction was maximally inhibited (Tmax) and 3) the width of the vagal effect curve at one-half the maximal amplitude (TD). Digoxin administration significantly (P less than .05) increased deltaPRmax, Tmax and TD by 21.6 +/- 4.3, 50.0 +/- 16.1 and 125.5 +/- 42.4 msec, respectively, before the disruption of sinus rhythm. Diluent or saline administration did not alter deltaPRmax, Tmax or TD. In addition, digoxin produced dose-dependent increases in deltaPRmax. These results suggest that digoxin vagal interactions not only affect the PR interval but also the time to the maximum delay in atrioventricular conduction and the length of time for depressed conduction after brief bursts of vagal activity.

Animals↗
PubMed1976

Role of the nervous system in experimentally induced arrhythmias.

The purpose of our studies was to examine the role of the nervous system in arrhythmias produced by digitalis overdose and coronary artery occlusion in the cat. This was done by observing the effect of these arrhythmogenic procedures on cardiac efferent neural activity and then determining whether any observed alteration in neural activity contributed to the cardiac rhythm disturbances evoked by digitalis and coronary artery occlusion. Our data indicate that both procedures used to evoke arrhythmias activate each division of the autonomic nervous system. Activation of the sympathetic nervous system resulted in a deleterious effect on cardiac rhythm whereas activation of the parasympathetic nervous system, in general, resulted in a beneficial effect on cardiac rhythm. With coronary occlusion, the role exerted by the nervous system depended on the anatomic location of the involved myocardium. Studies directed at elucidating the mechanisms whereby the nervous system caused cardiac rhythm disturbances indicated that there may be an important difference between the antiarrhythmic efficacy of beta-adrenergic blockade and bilateral stellate ganglionectomy. The latter procedure proved to be a more effective way of removing deleterious sympathetic neural effects on the heart. In conclusion, our findings suggest that the development of new drugs for treating arrhythmias resulting from digitalis and coronary occlusion should be aimed at finding drugs that act to either depress central sympathetic outflow or enhance parasympathetic effects on the ventricle.

Animals↗
PubMed1976

Neuroexcitatory effects of digoxin in the cat.

The effect of intravenous injections of digoxin (20 mug/kg every 15 minutes) on spontaneously occurring activity in autonomic efferent nerves, motor nerves, afferent nerves, electrocardiogram and on arterial blood pressure was evaluated in chloralose-anesthetized cats. Administration of digoxin enhanced neural activity in pre- and postganglionic cardiac synpathetic nerves and this enhancement occurred near the time the disturbances in ventricular rhym were noted. Neural activity continued to increase during ventricular tachycardia and maximum enhancement was observed just proir to ventricular fibrillation. Similar results were observed when digoxin was administered to animals in which neural activity was recorded from preganglionic splanchnic and superior cervical nerves. Digoxin administration also increased discharge frequency from vagus (efferent fibers), phrenic and carotid sinus nerves. Denervation of cardiovascular reflexogenic areas prevented the increased discharge in vagus nerves, reduced it in phrenic nerves, but did not affect nerve discharge in sympathetic nerves. These results suggest that digoxin-induced hyperactivity in synpathetic nerves was related to a central nervous system effect of the drug, whereas the mechanism for the digoxin-induced hyperactivity in vagus nerves involved a peripheral reflex effect of the drug. Both sites were involved in the digoxin-induced hyperactivity in phrenic nerves. Enhancement of cardiac sympathetic nerve activity appeared to be responsible for the ventricular arrhythmias provoked by digoxin as 1) a temporal relationship was observed between augmented nerve activity and arrhythmia development, 2) a centrally acting sympathetic nervous system depressant drug, clonidine, converted the ventricular arrhythmia to normal rhythm, and 3) removal of sympathetic influence to the heart by spinal cord transection decreased the sensitivity of the heart to the arrhythmogenic effect of digoxin. These results suggest that digoxin partially responsible for its cardiotoxic effects.

Adrenal Glands↗